Fig. 7

Infiltration of immune cells and vessel damage in the ischemic brain were suppressed by intranasal administration of PAD inhibitor. a Cl-amidine (5 mg/kg) was administered intranasally after 3 h of MCAO and levels of CitH3 and numbers and morphology of microglia and blood vessels were examined after 1, 2, or 4 d of MCAO. b CitH3 levels in cortices of ischemic hemispheres after 1 or 2 d of MCAO were determined by immunoblotting using GAPDH as a loading control. c-f Coronal brain sections were prepared after 4 d of MCAO and stained with anti-Iba-1 (c), anti-F4/80 (d), or anti-laminin antibody (e). Numbers of Iba-1-positive (C, 250 μm × 250 μm) and F4/80-positive cells (D, 250 μm × 250 μm) in cortex (Ct) and striatum (St) were counted and presented as means±SEMs. Total vessel length (E, 500 μm × 500 μm) and vessel density are presented as means±SEMs (F). Scale bars in C represent 200 μm and those in D, E represent 100 μm. Sham, sham-operated animals (n = 9 from 3 animals); MCAO+PBS, PBS-treated MCAO control animals (n = 12 from 4 animals); MCAO+Cl-amidine, the Cl-amidine-administered MCAO animals (n = 12 from 4 animals). Ct, cortex; St, striatum; Lm, leptomeninges. **p, < 0.01 vs. MCAO+PBS controls